Central Retinal Artery Occlusion

Introduction

Background

In 1859, Van Graefe first described central retinal artery occlusion (CRAO) as an
embolic event to the central retinal artery in a patient with endocarditis. In 1868,
Mauthner suggested that spasmodic contractions could lead to retinal artery
occlusion. There is a multitude of causes of CRAO, but patients typically present
with sudden, severe, and painless loss of vision.

Pathophysiology

Visual loss from CRAO occurs from the loss of blood supply to the inner layer of the
retina. The ophthalmic artery is the first branch of the internal carotid artery and
enters the orbit underneath the optic nerve through the optic canal. The central
retinal artery is the first intraorbital branch of the ophthalmic artery, which enters
the optic nerve 8-15 mm behind the globe to supply the retina. Short posterior
ciliary arteries branch distally from the ophthalmic artery and supply the choroid.
Anatomical variants include cilioretinal branches from the short posterior ciliary
artery, which gives additional supply to the macula from the choroidal circulation. A
cilioretinal artery occurs in approximately 14% of the population.

Acutely, obstruction of the central retinal artery results in inner layer edema and
pyknosis of the ganglion cell nuclei. Ischemic necrosis results, and the retina
becomes opacified and yellow-white in appearance. The opacity is most dense in
the posterior pole as a result of the increased thickness of the nerve fiber layer and
ganglion cells in this region. Furthermore, the foveola assumes a cherry-red spot
because of a combination of 2 factors: (1) the intact retinal pigment epithelium and
choroid underlying the fovea, and (2) the foveolar retina is nourished by the
choriocapillaris. The late stage shows a homogenous scar replacing the inner layer
of the retina.

Approximately 14% of the general population has cilioretinal arteries and 25% of
eyes with acute CRAO have cilioretinal artery. The cilioretinal artery supplies part or
all of papillomacular bundle. In 10% of eyes, the cilioretinal artery supplies some or
all of the foveola. In such an eye, the visual acuity generally returns to 20/50 or
better in 80% of eyes over a 2-week period.

The opacification takes as little as 15 minutes to several hours before becoming

evident and resolves in 4-6 weeks. The resulting anatomy reflects a catastrophic
insult to the inner retinal layers with attenuated retinal arterioles and optic nerve
pallor. Pigmentary changes are typically absent since the retinal pigment epithelium
remains unaffected. Boxcar appearance of the blood column can be seen in both
arteries and veins. Hayreh has shown that irreversible cell injury occurs after 90-
100 minutes of total CRAO in the primate model.1 Controversy exists regarding the
optimal window of treatment in humans, but the conservative approach involves
treatment up to 24 hours.

Frequency

United States

CRAO is found in 1 per 10,000 outpatient visits. Of these patients, 1-2% present
with bilateral involvement.

Mortality/Morbidity

Patients with visualized retinal artery emboli, whether or not obstruction is present,
have a 56% mortality rate over 9 years, compared to 27% for an age-matched
population without retinal artery emboli. Life expectancy of patients with CRAO is
5.5 years compared to 15.4 years for an age-matched population without CRAO.

Sex

Men are affected slightly more frequently than women.

Age

The mean age of presentation is in the early 60s, although a few cases have been
reported in patients younger than 30 years. The etiology of occlusion changes
depending on the age of presentation.

Clinical

History

• The most common presenting complaint is an acute, persistent, painless loss

of vision in the range of counting fingers to light perception in 90% of
patients. Consider ophthalmic artery occlusion if visual acuity is worse.

• Some patients may reveal a history of amaurosis fugax involving transient

loss of vision lasting seconds to minutes but which may last up to 2 hours.
The vision usually returns to baseline after an episode of amaurosis fugax.

• Ask about symptoms of temporal arteritis in the older population. Patients

complain of sudden, painless, nonprogressive vision loss in one eye. History
of headaches, jaw claudication, scalp tenderness, proximal muscle and joint
aches, anorexia, weight loss, or fever may be elicited.

• Ask about any medical problems that could predispose to embolus formation
(eg, atrial fibrillation, endocarditis, coagulopathies, atherosclerotic disease,
hypercoagulable state).
 • Prolonged direct pressure to the globe during drug-induced stupor or
improper positioning during surgery may lead to CRAO.

• Ask about drug history.

Physical

• Determine the degree of vision loss (eg, no light perception, hand movement,
counting fingers).

• Ocular examination includes the following:

o Check for afferent pupillary defect.

o Perform an optic nerve examination to look for signs of temporal

arteritis. Critical signs include afferent pupillary defect and
pale/swollen optic nerve with splinter hemorrhages.

o Cherry-red spot and a ground-glass retina may take hours to develop.

o The funduscopic findings typically resolve within days to weeks of the

acute event, sometimes leaving a pale optic disc as the only physical
finding.

o Emboli can be seen in about 20% of patients with CRAO.

o Boxcar segmentation can be seen in both arteries and veins. This is a

sign of severe obstruction.

o Perform a cardiovascular examination for murmurs or carotid bruits.

o Perform a systemic examination for temporal tenderness, jaw

claudication, muscle weakness, and fever to evaluate for temporal
arteritis.

Causes

Causes of CRAO vary depending on the age of the patient. A detailed analysis of
comorbid disease is necessary to elucidate the cause of the acute visual loss.

• Systemic hypertension seen in two thirds of patients

• Diabetes mellitus

• Cardiac valvular disease seen in one fourth of patients

• Cardiac anomalies, such as patent foramen ovale

• Embolism
 o This is most commonly cholesterol but can be calcific, bacterial, or talc
from intravenous drug abuse.

o This is associated with poorer visual acuity and higher morbidity and
mortality.

o Emboli from the heart are the most common cause of CRAO in patients
younger than 40 years.

o Amaurosis fugax preceding persistent loss of vision suggests branch

retinal artery occlusion (BRAO) or temporal arteritis and may represent
emboli causing temporary occlusion of the retinal artery.

o Coagulopathies from sickle cell anemia or antiphospholipid antibodies

are more common etiologies for CRAO in patients younger than 30
years.

• Atherosclerotic changes

o Carotid atherosclerosis is seen in 45% of cases of CRAO, with 60% or

greater stenosis in 20% of cases.

o Atherosclerotic disease is the leading cause of CRAO in patients aged

40-60 years.

• Giant cell arteritis

o Giant cell arteritis should be considered in patients older than 65

years, but do not ignore in younger patients.

o Giant cell arteritis may produce CRAO or ischemic optic neuropathy.

o Giant cell arteritis needs to be treated to preserve vision in the fellow

eye.

• Hypercoagulable state

• Collagen vascular disease

• Oral contraceptives

• Polycythemia

• Polyarteritis nodosa

• Rare causes

• Consider in younger patients

 • Behçet disease

• Syphilis

• Sickle cell disease

• Migraine

• Increased intraocular pressure from glaucoma or prolonged direct pressure to

the globe in unconscious patients

• Hydrostatic arterial occlusion

Differential Diagnoses

Retinopathy, Purtscher

Other Problems to Be Considered

Inadvertent intraocular injection of gentamicin

Arteritic ischemic optic neuropathy
Other causes of cherry-red spot
Tay-Sach disease or other storage disease

Workup

Laboratory Studies

• Laboratory studies are helpful in determining the etiology of central retinal

artery occlusion (CRAO).

o CBC count to evaluate anemia, polycythemia, and platelet disorders

o Erythrocyte sedimentation rate (ESR) evaluation for giant cell arteritis

o Fibrinogen, antiphospholipid antibodies, prothrombin time/activated

partial thromboplastin time (PT/aPTT), and serum protein
electrophoresis to evaluate for coagulopathies

o Fasting blood sugar, cholesterol, triglycerides, and lipid panel to

evaluate for atherosclerotic disease

o Blood cultures to evaluate for bacterial endocarditis and septic emboli

Imaging Studies

• Imaging studies are helpful in determining the etiology of CRAO.

• Carotid ultrasound imaging to evaluate atherosclerotic disease. This appears

to be more sensitive than carotid Doppler, which only determines the flow.
 • Magnetic resonance angiogram may be more accurate in detecting
obstruction.

• Fluorescein angiogram

o Delay in arteriovenous transit time (<11 seconds is in the reference

range)

o Delay in retinal arterial filling

o Normal choroidal filling (begins 1-2 seconds before retinal filling and
completely filled within 5 seconds of dye appearance in healthy eyes).
A delay of 5 seconds or greater is seen in 10% of patients. Consider
ophthalmic artery occlusion or carotid artery obstruction if there is a
significant delay in choroidal filling.

o Arterial narrowing with normal fluorescein transit after recanalization

Other Tests

• ECG to evaluate for possible atrial fibrillation (A 24-h Holter monitor may be
necessary if arrhythmia is suspected but not detected on ECG testing.)

• Electroretinogram shows a diminished b-wave corresponding to Muller and/or

bipolar cell ischemia.

• Echocardiogram (not necessarily an emergency department test)

o To evaluate valvular disease, wall motion abnormalities, and mural

thrombi

o To evaluate vegetations that may cause septic emboli

Procedures

• The mainstay of therapy is procedure and pharmacologic therapy (see

Medical Care and Medication).

• Ocular massage

o Apply direct pressure for 5-15 seconds, then release. Repeat several
times.

o A fundus contact lens or digital massage may be used.

o Ocular massage can dislodge the embolus to a point further down the
arterial circulation and improve retinal perfusion.

• Anterior chamber paracentesis

 o Administer local anesthesia. Use a 30-gauge needle on a tuberculin
syringe.

o Enter the eye at the limbus with bevel up.

o Ensure that the needle does not damage the lens.

o Withdraw fluid until the anterior chamber shallows slightly (0.1-0.2 cc).

o Administer a postprocedure topical antibiotic.

o A decrease in intraocular pressure is believed to allow greater

perfusion, pushing emboli further down the vascular tree.

• Intra-arterial fibrinolysis

o This procedure is controversial.

o Limited evidence of improved visual acuity with urokinase is available.

A few cases of intra-arterial tissue plasminogen activator (tPA)
administration have been observed to be successful.

o Systemic complications include transient ischemic attack (TIA), stroke,

and hematoma.

Treatment

Medical Care

• Immediate lowering of intraocular pressure includes acetazolamide 500 mg IV

or 500 mg PO once.

• Topical medications are used to lower intraocular pressure.

• Further treatments

o Carbogen therapy (5% CO2, 95% O2): CO2 dilates retinal arterioles, and
O2 increases oxygen delivery to ischemic tissues. Perform for 10
minutes every 2 hours for 48 hours.

o Hyperbaric oxygen therapy (HBOT) may be beneficial if begun within 2-

12 hours of symptom onset. Institute treatment with other
interventions first, as transport to a chamber may usurp precious time.

Consultations

• Hyperbaric medicine
 o Early treatment (<2 h from onset of symptoms) with HBOT may be
associated with increased visual recovery, but HBOT can be considered
if the duration of visual loss is less than 12 hours.

o Inhalation of 100% oxygen at 2 atmospheric absolute provides an

arterial pO2 of 1000-1200 mm Hg, resulting in a 3-fold increase in
oxygen diffusion distance through ischemic retinal tissues. Some
studies show a 40% improvement of 2 or more levels of visual acuity.

Medication

Medical therapy is directed toward lowering IOP, increasing retinal perfusion, and
increasing oxygen delivery to hypoxic tissues. The first goal is accomplished by
using the same drugs as those used in glaucoma. Retinal perfusion may be
increased by vasodilatory drugs, increasing arterial pCO2, or by giving peripheral
thrombolytics to remove the offending embolus. Some also advocate aspirin use in
the acute phase. Oxygen delivery is improved by breathing higher concentrations of
oxygen or with hyperbaric oxygen.

Carbonic anhydrase inhibitors

Carbonic anhydrase is an enzyme found in many tissues of the body, including the
eye. The reversible reaction it catalyzes involves the hydration of carbon dioxide
and the dehydration of carbonic acid.

Acetazolamide (Diamox)

Reduces rate of aqueous humor formation by inhibiting enzyme carbonic

anhydrase, which results in decreased IOP. Used most frequently as single diuretic
agent in acute management of CRAO. Other diuretics may be added if sufficient
decrease in IOP is not attained.

Adult

250-500 mg IV; repeat in 2-4 h prn; not to exceed 1 g/d

Pediatric

10-15 mg/kg/d PO divided q6-8h

5-10 mg/kg/dose IV/IM q6h

Dorzolamide (Trusopt)

Used concomitantly with other topical ophthalmic drug products to lower IOP. If
more than one ophthalmic drug is being used, administer the drugs at least 10 min
apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at
renal tubule and increases renal excretion of sodium, potassium bicarbonate, and
water to decrease production of aqueous humor.

Adult

1 gtt tid in affected eye(s)

Pediatric

Not established

Hyperosmotic diuretics

Lower IOP by creating an osmotic gradient between the ocular fluids and plasma
(not for long-term use).

Mannitol (Osmitrol)

Reduces elevated IOP when the pressure cannot be lowered by other means.
Initially assess for adequate renal function in adults by administering a test dose of
200 mg/kg, given IV over 3-5 min. It should produce a urine flow of at least 30-50
mL/h of urine over 2-3 h. In children, assess for adequate renal function by
administering a test dose of 200 mg/kg, given IV over 3-5 min. It should produce a
urine flow of at least 1 mL/h over 1-3 h.

Adult

1.5-2 g/kg IV as a 20% solution (7.5-10 mL/kg) or as a 15% solution (10-13 mL/kg)
over a period as short as 30 min

Pediatric

Initial dose: 0.5-1 g/kg IV

Maintenance dose: 0.25–0.5 g/kg IV q4-6h

Glycerin

Used in glaucoma to interrupt acute attacks. Oral osmotic agent for reducing IOP.
Able to increase tonicity of blood until finally metabolized and eliminated by the
kidneys. Maximum reduction of IOP usually occurs 1 h after glycerin administration.
Effect usually lasts approximately 5 h.

Adult

1-2 g/kg PO; repeat q5h prn

Alternatively, 1 mL/kg PO as a 50% solution in juice
Pediatric

Administer as in adults

Sympathomimetics

Lower IOP mainly by increasing outflow and reducing the production of aqueous
humor. The combination of a miotic and a sympathomimetic has additive effects in
lowering IOP. Each may be added in rotation after a 5-minute interval, until target
IOP is reached.

Apraclonidine (Iopidine)

Reduces elevated, as well as normal, IOP whether or not accompanied by glaucoma.

Apraclonidine is a relatively selective alpha-adrenergic agonist that does not have
significant local anesthetic activity. Has minimal cardiovascular effects.

Adult

Solution (0.5%): 1-2 gtt in affected eye(s) tid; since apraclonidine 0.5% will be used
with other ocular glaucoma therapies, use an approximate 5-min interval between
instillation of each medication to prevent washout of previous dose; do not inject
into the eye
Solution (1%): 1 gtt in affected eye 1 h before initiating anterior segment laser
surgery; second gtt into the same eye immediately upon completion of surgery

Pediatric

Not established

Dipivefrin (AKPro, Propine)

Converted to epinephrine in eye by enzymatic hydrolysis. Appears to act by

decreasing aqueous production and enhancing outflow facility. Has same
therapeutic effect as epinephrine with fewer local and systemic side effects. May be
used as an initial therapy or as an adjunct with other antiglaucoma agents for the
control of IOP.

Adult

1 gtt into eye(s) q12h

Pediatric

Not established

Beta-adrenergic blocking agents

Lower IOP by decreasing the rate of aqueous humor production and possibly
outflow. They may be more effective than either pilocarpine or epinephrine alone
and have the advantage of not affecting pupil size or accommodation.

Timolol (Timoptic)

May reduce elevated and normal IOP, with or without glaucoma by reducing the
production of aqueous humor or by outflow.

Adult

1 gtt of 0.25% or 0.5% in affected eye(s) bid; if IOP is maintained at satisfactory

levels, change the dosage to 1 gtt in affected eye(s) qd; if clinical response is not
adequate, change dosage to 1 gtt of 0.5% solution in affected eye(s) bid; if IOP is
still not at a satisfactory level, consider concomitant therapy

Pediatric

Administer as in adults

Corticosteroids

Used in arterial occlusion only when temporal arteritis (GCA) is the suspected or
confirmed etiology.

Prednisone (Deltasone, Orasone, Meticorten)

Useful in the treatment of inflammatory and allergic reactions. May decrease

inflammation by reversing increased capillary permeability and suppressing
polymorphonuclear lymphocyte activity.

Adult

5-60 mg PO qd or divided bid/qid; not to exceed 80 mg/d; taper over 2 wk as

symptoms resolve
Once giant cell arteritis is suspected, administer methylprednisolone, 250 mg IV
q6h for 12 doses; then, switch to prednisone, 80-100 mg PO qd; adjust dose
clinically

Pediatric

4-5 mg/m2/d PO
Alternative: 1-2 mg/kg PO qd; taper over 2 wk as symptoms resolve

Follow-up

Further Inpatient Care

 • Inpatient care is indicated only if comorbid disease is present.

Further Outpatient Care

• A follow-up ophthalmic examination should be performed 1-4 weeks after the

event to check for neovascularization of the disc or iris.

o Neovascularization of the iris occurs in 20% of patients at an average

of 4-5 weeks after the event. The range is 1-15 weeks. Panretinal
photocoagulation is effective in causing regression of iris
neovascularization in 65% of patients.

o Neovascularization of the disc occurs in 2-3% of patients. Panretinal

photocoagulation is effective for optic disc neovascularization.

• A complete systemic workup should be performed by a primary care provider.

• If hyperbaric oxygen therapy (HBOT) is to be used, several treatments may

be necessary.

Inpatient & Outpatient Medications

• In/out patient medications are indicated only if comorbid disease is present.

Transfer

• Transfer to a hyperbaric facility is necessary if HBOT is to be administered.

Deterrence/Prevention

• Patients should control their blood pressure, lower their cholesterol, avoid
intravenous drugs, and take their medication.

Complications

• Further emboli to the brain resulting in a cerebrovascular accident

• Further emboli to the same or contralateral eye, resulting in further visual

loss

• Progression of temporal arteritis, resulting in loss of vision to the contralateral

eye

Prognosis

• Most patients continue to experience severe vision loss in the counting

fingers to hand motion range.
 • As many as 10% of patients retain central vision because of the presence of a
cilioretinal artery. In this case, visual acuity improves to 20/50 or better in
80% of cases over a 2-week period.

• The presence of a retinal embolus is associated with a 56% mortality rate

over 9 years compared to 27% in patients without arterial emboli.

• Life expectancy of patients with central retinal artery occlusion (CRAO) is 5.5
years compared to 15.4 years for an age-matched population without CRAO.

Patient Education

• Patients must understand that the prognosis for visual recovery is poor and
that the visual changes are usually a result of a systemic process that needs
treatment.

Miscellaneous

Medicolegal Pitfalls

• Failure to perform a workup of the systemic cause of CRAO, leading to a

progression of disease or recurrence of symptoms

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